Abstract: FR-PO0244
CCL7 Inhibition Ameliorates Renal Fibrosis Through Activating Inflammation and Epithelial-Mesenchymal Transition in a Mouse Model of Unilateral Ureteral Obstruction
Session Information
- CKD: Mechanisms of Injury and Fibrosis - 2
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: CKD (Non-Dialysis)
- 2203 CKD (Non-Dialysis): Mechanisms
Authors
- Lee, Hsin Jou, National Yang Ming Chiao Tung University School of Medicine, Taipei City, Taiwan
- Chiang, Chih-Hung, Taipei Municipal United Hospital System, Taipei City, Taiwan
- Chang, Ting-Ting, National Yang Ming Chiao Tung University School of Medicine, Taipei City, Taiwan
Background
Chronic kidney disease (CKD) affects approximately 700 million people worldwide. As CKD progress, renal fibrosis, characterized by excessive extracellular matrix deposition in the kidney, irreversibly leads to end-stage renal failure. Chemokine C-C motif ligand 7 (CCL7), also known as monocyte chemoattractant protein 3, functions as a chemoattractant of monocytes. CCL7 has been reported to be upregulated in several kidney diseases. The study aimed to investigate the direct role of CCL7 in renal fibrosis.
Methods
Mice were subjected to unilateral ureteral obstruction (UUO) to cause renal fibrosis. CCL7 expression was inhibited through the administration of CCL7-specific antibodies or by employing genetic knockout techniques. Serum blood urea nitrogen (BUN) and creatinine levels were measured. Kidney sections were analyzed by Hematoxylin and eosin, periodic acid–Schiff, and Masson's trichrome staining. Serum CCL7 concentration was determined by CCL7 ELISA kits. Protein levels were analyzed by Western blotting.
Results
Serum level and the protein expression of CCL7 were elevated in UUO mice, and they were decreased by the injection of CCL7 antibodies or gene deletion. Administration of CCL7 antibodies or gene deletion protected renal function, as evidenced by reduced BUN and creatinine levels in UUO mice. In parallel, histological analysis of the kidney showed that glomerulosclerosis, tubulointerstitial fibrosis, and collagen deposition were attenuated following the CCL7 inhibition. Mechanistically, the protein expression of inflammatory cytokines as well as epithelial-mesenchymal transition (EMT) markers were reduced in the kidneys of CCL7-inhibited UUO mice.
Conclusion
CCL7 plays an important role in the pathology of renal fibrosis by regulating inflammation and EMT processes. Although further clinical studies are warranted, these findings suggest that the inhibition of CCL7 may be a potential therapeutic strategy for CKD.
Acknowledgment
This study was supported by the National Science and Technology Council (NSTC), Taiwan.